m6A regulator-mediated methylation modifications define the immune infiltration characteristics of the tumor microenvironment in prostate adenocarcinoma

Prostate adenocarcinoma (PRAD) persists as the predominant non-cutaneous malignancy diagnosed in males, which is a primary contributor to cancer-related mortality globally. It is reported that the progression of prostate adenocarcinoma is associated with various factors, including genetics, age, obesity, etc. Contemporary research indicates that epigenetic inheritance is a leading factor in the initiation and progression of cancer. RNA methylation modification is the most prevalent form of RNA modification, with N6-methyladenosine (m6A) representing the most common modification on mRNA and lncRNAs. However, the biological mechanisms underpinning this association in prostate adenocarcinoma and its correlation with patients' prognostic survival outcomes remain elusive. Our study elucidates the roles of the tumor microenvironment (TME) and genetic mutations during the initiation and progression of prostate adenocarcinoma. Additionally, we stratify prostate adenocarcinoma into distinct subtypes based on m6A scoring. This approach enhances our comprehension of the functional role of m6A in the development of prostate adenocarcinoma, offering novel insights into the clinical strategies and understanding the biological significance between prostate adenocarcinoma and m6A modification.